These results suggest that the GSTT1 and GSTM1 null genotypes and the GSTP1 Val/Val polymorphism may play important roles in asthma pathogenesis. It is possible that intermediate electrophilic metabolites, arising in the first phase of detoxification, are not metabolized by GST enzymes in asthmatic patients and are not excreted. These intermediate metabolites may damage cells and generate oxidative stress, and so contribute to the pathogenesis of asthma.

Background: Leptin is a protein mainly secreted by adipocytes, and the major function of leptin was its role in body weight regulation. In humans, there was a strong correlation between leptin and nutritional parameters, such as body mass index (BMI) and fat mass (FM). Administration of recombinant leptin to ob/ob mice, which have a genetic defect in leptin production, reduces food intake, increases energy expenditure, and decreases body weight. It is suggested that increased levels of circulating leptin levels may contribute to anorexia and weight loss in pathologic conditions including chronic obstructive pulmonary disease (COPD). Recent studies have provided evidence for a link between leptin and proinflammatory cytokines such as TNF-α. Objective: This study aimed to detect serum leptin and TNF-α levels in COPD patients without weight loss during stable disease and acute exacerbation, and to investigate relationships between leptin, TNF-α and nutritional parameters at different stages of the disease. Material and Methods: 26 stable COPD patients, 16 COPD patients with acute exacerbation and 15 control subjects participated in this study. To eliminate the effects of sex differences, all patients and controls were male. BMI, percent ideal body weight, percent FM, sum of skinfold tickness and serum leptin and TNF-α levels were measured in all participants. Leptin and TNF-α levels were measured by ELISA. Results: Serum leptin and TNF-α levels were significantly higher in the patients experiencing exacerbation than in the stable patients and controls. Although leptin levels were lower and TNF-α levels were higher in the stable patient group than in the controls, these differences were not statistically different. Leptin levels were significantly correlated with the nutritional parameters in both control and stable groups. However, in patients with acute exacerbation, a correlation between leptin and nutritional parameters was not found. There was no significant relationship between TNF-α and nutritional parameters in the three groups. In addition, while there was no correlation between leptin and TNF-α levels in the stable and control groups, a significant positive correlation was observed in patients with exacerbation. Conclusion: In conclusion (1) elevated TNF-α levels may be related to increased inflammation in patients, (2) circulating TNF-α levels were associated with increased leptin levels and (3) although leptin and nutritional parameters were correlated in the stable COPD patients, the correlation was weaker compared to controls, and during an exacerbation it disappeared completely. Therefore, inappropriately increased levels of leptin and TNF-α noted during recurrent acute exacerbations in patients with COPD may lead to changes in nutritional parameters and body weight in the course of the disease.

We found that the prevalence of asthma was more common in the IBS group than in controls. Our finding supports the speculation that asthma and IBS may share common pathophysiological processes.

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There is an increasing interest in the concept that oxidant/antioxidant imbalance plays a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, most of the studies are concentrated on the local antioxidant/oxidant balance. In this study, we investigated the oxidant/antioxidant balance in systemic circulation of patients with COPD. Serum malonyldialdehyde (MDA), vitamin C and erythrocyte reduced glutathione (GSH) were determined in patients during acute exacerbation and during the stable phase of the disease, and compared with age- and sex-matched healthy controls. The levels of serum MDA, vitamin C and erythrocyte GSH were determined according to Yagi, Beutler and Bauer et al., respectively. Serum MDA levels were significantly higher in patients compared to controls, and during acute exacerbation compared to the stable phase. MDA levels in patients with acute exacerbation and in those in stable phase were also higher than in controls. We found significantly decreased levels of erythrocyte GSH and serum vitamin C in patients with acute exacerbation and stable COPD compared to controls. Although smoking caused an increase in oxidative stress in controls, the measured parameters were not affected by smoking in the patient group. In conclusion, there is a systemic oxidant/antioxidant imbalance in COPD, and this imbalance is probably independent of smoking.